Farnesyltransferase inhibition causes morphological reversion of ras-transformed cells by a complex mechanism that involves regulation of the actin cytoskeleton.
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Prenylated prelamin A interacts with Narf, a novel nuclear proteinRasGRP4 is a novel Ras activator isolated from acute myeloid leukemiaA new member of the Rho family, Rnd1, promotes disassembly of actin filament structures and loss of cell adhesionRhoB alteration is necessary for apoptotic and antineoplastic responses to farnesyltransferase inhibitorsNew targets for therapy in breast cancer: farnesyltransferase inhibitors.The farnesyl transferase inhibitor RPR-130401 does not alter radiation susceptibility in human tumor cells with a K-Ras mutation in spite of large changes in ploidy and lamin B distributionInteraction Between Mevalonate Pathway and Retinoic Acid-Induced DifferentiationRas-induced cellular events (review)Protein farnesyltransferase inhibitors block the growth of ras-dependent tumors in nude miceNf1-deficient mouse Schwann cells are angiogenic and invasive and can be induced to hyperproliferate: reversion of some phenotypes by an inhibitor of farnesyl protein transferaseRhoB is dispensable for mouse development, but it modifies susceptibility to tumor formation as well as cell adhesion and growth factor signaling in transformed cellsRig is a novel Ras-related protein and potential neural tumor suppressorThe farnesyltransferase inhibitor, FTI-2153, blocks bipolar spindle formation and chromosome alignment and causes prometaphase accumulation during mitosis of human lung cancer cells.Phase I and pharmacological study of the farnesyltransferase inhibitor tipifarnib (Zarnestra, R115777) in combination with gemcitabine and cisplatin in patients with advanced solid tumoursA phase II study of the farnesyl transferase inhibitor, tipifarnib, in children with recurrent or progressive high-grade glioma, medulloblastoma/primitive neuroectodermal tumor, or brainstem glioma: a Children's Oncology Group study.Farnesyltransferase inhibitors. Preclinical development.Characterization of farnesylated protein tyrosine phosphatase TcPRL-1 from Trypanosoma cruziA farnesyltransferase inhibitor induces tumor regression in transgenic mice harboring multiple oncogenic mutations by mediating alterations in both cell cycle control and apoptosis.Farnesyltransferase and geranylgeranyltransferase I inhibitors and cancer therapy: lessons from mechanism and bench-to-bedside translational studies.Ras farnesyltransferase inhibitors suppress the phenotype resulting from an activated ras mutation in Caenorhabditis elegans.Inhibiting signal transduction: recent advances in the development of receptor tyrosine kinase and Ras inhibitors.High-content profiling of cell responsiveness to graded substrates based on combinyatorially variant polymersFarnesyltransferase inhibitors in breast cancer therapy.Molecular biological design of novel antineoplastic therapies.Phase I study of S-trans, trans-farnesylthiosalicylic acid (salirasib), a novel oral RAS inhibitor in patients with refractory hematologic malignancies.Massive programmed cell death in intestinal epithelial cells induced by three-dimensional growth conditions: suppression by mutant c-H-ras oncogene expressionReversal of the Ras-induced transformed phenotype by HR12, a novel ras farnesylation inhibitor, is mediated by the Mek/Erk pathway.Inhibition of farnesyltransferase: a rational approach to treat cancer?Anti-infectives targeting the isoprenoid pathway of Toxoplasma gondii.Farnesyltransferase inhibitors induce dramatic morphological changes of KNRK cells that are blocked by microtubule interfering agents.Novel tricyclic inhibitors of farnesyl protein transferase. Biochemical characterization and inhibition of Ras modification in transfected Cos cells.Evidence that farnesyltransferase inhibitors suppress Ras transformation by interfering with Rho activity.Cell growth inhibition by farnesyltransferase inhibitors is mediated by gain of geranylgeranylated RhoB.Smad3 deficiency inhibits v-ras-induced transformation by suppression of JNK MAPK signaling and increased farnesyl transferase inhibition.Tamoxifen and the farnesyl transferase inhibitor FTI-277 synergize to inhibit growth in estrogen receptor-positive breast tumor cell lines.Cdk inhibitors, roscovitine and olomoucine, synergize with farnesyltransferase inhibitor (FTI) to induce efficient apoptosis of human cancer cell lines.Suppression of malignant growth potentials of v-Src-transformed human gallbladder epithelial cells by adenovirus-mediated dominant negative H-Ras.Inhibition of DNA synthesis by a farnesyltransferase inhibitor involves inhibition of the p70(s6k) pathway.Membrane interactions of a constitutively active GFP-Ki-Ras 4B and their role in signaling. Evidence from lateral mobility studies.Farnesyltransferase inhibitors and anti-Ras therapy.
P2860
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P2860
Farnesyltransferase inhibition causes morphological reversion of ras-transformed cells by a complex mechanism that involves regulation of the actin cytoskeleton.
description
1994 nî lūn-bûn
@nan
1994年の論文
@ja
1994年論文
@yue
1994年論文
@zh-hant
1994年論文
@zh-hk
1994年論文
@zh-mo
1994年論文
@zh-tw
1994年论文
@wuu
1994年论文
@zh
1994年论文
@zh-cn
name
Farnesyltransferase inhibition ...... ion of the actin cytoskeleton.
@en
type
label
Farnesyltransferase inhibition ...... ion of the actin cytoskeleton.
@en
prefLabel
Farnesyltransferase inhibition ...... ion of the actin cytoskeleton.
@en
P2093
P2860
P356
P1476
Farnesyltransferase inhibition ...... ion of the actin cytoskeleton.
@en
P2093
Giuliani EA
Prendergast GC
deSolms SJ
P2860
P304
P356
10.1128/MCB.14.6.4193
P407
P577
1994-06-01T00:00:00Z